Boundary Flow-Induced Membrane Tubulation Under Turgor Pressures

被引:0
作者
Xue, Hao [1 ]
Ma, Rui [1 ,2 ]
机构
[1] Xiamen Univ, Dept Phys, Xiamen 361005, Peoples R China
[2] Xiamen Univ, Fujian Prov Key Lab Soft Funct Mat Res, Xiamen 361005, Peoples R China
基金
中国国家自然科学基金;
关键词
endocytosis; membrane dynamics; boundary flow; FORCE GENERATION; ACTIN; ENDOCYTOSIS; VESICLES; YEAST; INSTABILITY; MECHANISMS; CURVATURE; TENSION;
D O I
10.3390/membranes15040106; 10.3390/membranes15040106
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
During clathrin-mediated endocytosis in yeast cells, a small patch of flat membrane is deformed into a tubular shape. It is generally believed that the tubulation is powered by actin polymerization. However, studies based on quantitative measurement of the actin molecules suggest that they are not sufficient to produce the forces to overcome the high turgor pressure inside of the cell. In this paper, we model the membrane as a viscous 2D fluid with elasticity and study the dynamic membrane deformation powered by a boundary lipid flow under osmotic pressure. We find that in the absence pressure, the lipid flow drives the membrane into a spherical shape or a parachute shape. The shapes over time exhibit self-similarity. The presence of pressure transforms the membrane into a tubular shape that elongates almost linearly with time and the self-similarity between shapes at different times is lost. Furthermore, the width of the tube is found to scale inversely to the cubic root of the pressure, and the tension across the membrane is negative and scales to the cubic root squared of the pressure. Our results demonstrate that boundary flow powered by myosin motors, as a new way to deform the membrane, could be a supplementary mechanism to actin polymerization to drive endocytosis in yeast cells.
引用
收藏
页数:17
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